Schneider J, Panne E, Braun H, Mordasini R, Kaffarnik H
J Lab Clin Med. 1983 Jan;101(1):114-22.
Ethanol produces a number of effects in different steps of lipid metabolism which have been suggested to be responsible for the common phenomenon of ethanol-induced hyperlipoproteinemia in man. The occurrence of hyperchylomicronemia has been attributed to an ethanol-specific disturbance of the clearing mechanism of triglyceride-rich lipoproteins. However, the reports on lipolytic activities and the clearance of chylomicrons after ethanol ingestion are contradictory. In this investigation the short-term excess of serum lipoproteins and the lipolytic activities in healthy volunteers were studied after single and prolonged ethanol ingestion followed by an intravenous lipid load. One hour after a single oral dose of ethanol, the intravenous fat tolerance test was unchanged. After an ethanol load over a 5 hr period, the fat tolerance was reduced, although the same ethanol levels at the time of infusion were maintained. In addition, the lipolytic activities of the serum were significantly reduced after 5 hr of ethanol ingestion followed by intravenous fat load. Hence the time relations between ethanol and fat loads determine whether a defect in chylomicron catabolism can be observed or not. A striking difference in the situations when the fat infusions were performed was the development of endogenous hypertriglyceridemia after 5 hr of ethanol ingestion. Since ethanol-dependent differences in the absorption of fat are ruled out by our experimental design, we attribute our findings to a competitive inhibition of chylomicron degradation by VLDL and partial depletion of the lipolytic system by combined endogenous and exogenous hypertriglyceridemia.